Traumatic Brain Injury (TBI) is a major public health problem. Since 2001, over 150,000 US military personnel have been diagnosed with a mild form of TBI, often after exposure to an explosive blast (bTBI), with a spectrum of neurological and psychological deficits.
The Centers for Disease Control and Prevention (CDC) separates blast injury into four phases. The primary injury phase is the response of brain tissue to the blast wave from an intense over-pressurization impulse of the blast. A secondary injury phase results from shrapnel penetration. Tertiary injury is caused by head contact/acceleration forces as the body is moved by the forced air flow from the blast. A quaternary injury phase is any injury not included in the first three phases, such as hemorrhagic shock or chemical/thermal burn injury.
The primary injury phase, the direct result of the shockwave generated by an explosion, is the least understood. The blast shock wave (BSW) of primary bTBI is a transient, solitary supersonic pressure wave with a rapid (sub-msec) increase in pressure (i.e. compression) followed by a more slowly developing (msec) rarefraction phase of low pressure (i.e. tension). In the majority of bTBI, the peak pressure is low; exposure to blasts estimated to create 10 atm peak pressure in the skull for a few milliseconds can result in death for unprotected persons. Although dynamic compression, tension, and shear stress have all been proposed to explain primary bTBI, the identity of the mechanical forces involved, the tissue-force interaction(s) and the cellular damage properties remain unresolved.
A barotrauma chamber is commonly used to study the effect of pressure on biological tissue, such as CNS tissue. Shepard et al., J. Surg. Res. 51:417-424 (1991). The barotrauma chamber applies pressure evenly to all cells or tissue components in the chamber. The pressure wave in a barotrauma chamber can be produced by either hydrostatic or fluid percussion mechanisms.
Extracorporeal shock wave lithotripsy (ESWL) has also been used to generate high-amplitude, transient pressure pulses to study shock-wave induced tissue damage. For example, Howard and Sturtevant used ESWL in vitro on thin membranes immersed in tissue-mimicking fluids to study the mechanism of pulsed pressure tissue damage. Ultrasound Med. Biol. 23:1107-1122 (1997). This device permitted the study of pressure-induced compression and lateral extension that induced shear damage to structures such as the plasma membrane, organelles and intracellular membranes.
Shock tubes have also been used to expose cells or even entire bodies to simulated blasts to study how they respond to fast and extreme changes in pressure, as in Arun et al., Neuroreport 22:379-384 (2011). A compression-driven shock tube was used to simulate blast effects and subsequently study neuropathological changes in Long et al., J. Neurotrauma 26:827-840 (2009). The blast overpressure was generated by introducing pressurized gas into the shock tube until a Mylar membrane ruptured at a preselected pressure.